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J H Oh

Publications and source records attributed to J H Oh.

77 records · Page 5Linked to original sources

Mechanisms of dynamic cardiomyoplasty: current concepts.

Dynamic cardiomyoplasty is an operation that is undergoing worldwide clinical evaluation. It had been developed to utilize the patient's own skeletal muscle to assist the failing heart. Although the clinical and quality of life benefits of cardiomyoplasty have been reported in most patients, the results of quantitative hemodynamic analyses have been less consistent. This has prompted the reevaluation of the mechanisms of dynamic cardiomyoplasty other than simple cardiac compression by the wrapped muscle. There is good evidence to suggest that the following, either together or in part, comprise some of the mechanisms of dynamic cardiomyoplasty: (1) direct systolic assist; (2) myocardial (wall stress) sparing effect; (3) remodeling/girdling effect; and (4) angiogenesis. Current concepts and potential additional mechanisms are discussed and integrated, based on a review of the literature and our own recent studies.

Cardiomyoplasty↗

Hemodynamic response to in situ latissimus dorsi muscle stimulation: implications in dynamic cardiomyoplasty.

Dynamic cardiomyoplasty (DCM) involves the electrical stimulation of a pedicled latissimus dorsi muscle flap wrapped around the falling ventricle as a means of cardiac assist. To further elucidate a potential neurohumoral mechanism for improvement of cardiac output after myoplasty, we evaluated the hemodynamic effects of in situ stimulation of the latissimus dorsi muscle (in the absence of cardiomyoplasty). In seven mongrel dogs, a nerve cuff electrode (Medtronic 6901) was placed around the left thoracodorsal nerve (TDN). This was attached to a pulse generator (Medtronic, Itrel 7420), delivering a 4.0 volt, 0.19 second on, 0.81 second off, 33 Hz, 210 microsecond pulse width, cyclic bursts similar to that used in DCM. Stroke volume index (SVI) and other hemodynamic parameters as well as plasma norepinephrine (NE) levels were measured at five stages: baseline, stimulator on at 0, 2, and 5 minutes, and stimulator off at 30 minutes after. The animals were then subjected to 4 weeks of rapid pacing at 240 beats/min (Medtronic 8329) to induce heart failure, and as the rapid pacing was discontinued, measurements were repeated as above. After rapid pacing, cardiac function was significantly depressed, and NE was elevated (133 +/- 69 versus 500 +/- 353 pg/mL, p < 0.05). In the normal hearts, TDN stimulation increased SVI, heart rate, systemic pressure, and NE levels. In heart failure, however, no significant changes in cardiac function and NE levels were noted. In conclusion, our data indicate that in the normal hearts, afferent impulses from TDN stimulation alone may augment cardiac function by means of a neurohumoral effect that is not seen in severe heart failure. The implications of these findings in DCM are discussed.

Animals↗

Effect of glycolic acid on UVB-induced skin damage and inflammation in guinea pigs.

OBJECTIVES: Recently the use of glycolic-acid-containing cosmetics has received increased public interest in their supposed ability to reduce wrinkles, roughness, age spots and other skin damage. However, the safety of such products when used excessively or chronically, especially by photosensitive people, is being questioned. The purpose of this study was to examine the effects of glycolic acid alone or in combination with UVB on skin damage and inflammatory response. METHOD: Guinea pigs were treated with glycolic acid (from 1 to 7 mg/cm(2)) alone or in combination with UVB (0.4 or 3 J/cm(2)) for 14 days. Skin damage was evaluated by scoring the skin irritation value by the method of Draize and by histopathological observations. Cyclooxygenase 2 (COX-2) expression and prostaglandin E(2) (PGE(2)) production were also assessed. RESULTS: Glycolic acid caused an increase in the level of skin damage in a dose- and time-dependent manner. Lower doses (1 and 3 mg/cm(2)) of glycolic acid mostly caused erythema and eschar, and these consequently formed scales, whereas higher doses (5 and 7 mg/cm(2)) of glycolic acid caused redness, edema and necrotic ulceration. Glycolic acid also increased the thickness of the epidermal layer, reduced the organization of the stratum corneum and eventually destroyed some parts of the epidermal layer at 7 mg/cm(2). UVB (0.4 and 3 J/cm(2)) caused redness and edema as well as reduced the integrity of the stratum corneum. Glycolic acid enhanced the UVB-induced skin damage. The magnitude of the damage caused by combined UVB and glycolic acid treatment was much greater than that caused by glycolic acid or UVB alone. Moreover, partial destruction of the epidermal layer was observed in skin treated with 3 J/cm(2) UVB and 3 mg/cm(2) glycolic acid. However, glycolic acid did not change the basal and UVB-induced PGE(2) production and COX-2 protein expression. CONCLUSION: These results show that glycolic acid causes skin damage in a dose- and time-dependent manner and that it enhances UVB-induced skin damage without accompanying PGE(2) production or COX-2 protein expression. Therefore, caution should be exercised by those using glycolic acid on a chronic basis or excessively. Moreover, those with photosensitive skins and those more exposed to the sun should be particularly careful.

Animals↗

Structural and functional alterations of the peritoneum after prolonged exposure to dialysis solutions: role of aminoguanidine.

OBJECTIVE: The effect of long-term use of high glucose dialysate on peritoneal structure and function, and its relation with accumulation of advanced glycosylation end-product (AGE) in the peritoneum was investigated in this study. METHODS: Dialysates with 4.25% glucose were injected into the peritoneal cavity of normal rats for 12 weeks without (PD, n = 7) and with (1 g/L, PD+AG, n = 7) aminoguanidine in their drinking water. Rats not having intraperitoneal (IP) injection served as control (n = 9). After 12 weeks of IP injection, a 2-hour peritoneal equilibration test (PET) was performed using 30 mL 4.25% glucose dialysate. Intraperitoneal volume (IPV), dialysate-to-plasma urea ratio at 2 hours (D/P2), the ratio of dialysate glucose at 2 hours to initial dialysate glucose (D2/D0), and the peritoneal fluid absorption rate (Qa) were evaluated. After the PET, samples of the parietal peritoneum were taken for hematoxylin and eosin (H&E) staining and immunohistochemical staining for AGE. RESULTS: The IPV and D2/D0 glucose were significantly lower and Qa and D2/P2 urea significantly higher in the PD group than in the control group. Aminoguanidine reversed in part the changes in IPV and D2/P2 urea in the PD group; it had no effect on Qa and D2/D0 glucose. The H&E staining showed a linear mesothelial lining with negligible cells and capillaries in the narrow submesothelial space in the control group. Mesothelial denudation and submesothelial infiltration of monocytes and capillary formation were observed in the PD group. Mesothelial denudation was relatively intact in the PD+AG group compared with the PD group. Submesothelial monocyte infiltration and capillary formation in the PD+AG group were not as prominent as in the PD group. Positive AGE staining was found in the submesothelial space, vascular walls, and endomysium in the PD group, while it was markedly attenuated in PD+AG group and negligible in the control group. CONCLUSION: Long-term use of high glucose solutions induced peritoneal AGE accumulation and mesothelial denudation, and increased peritoneal permeability and peritoneal fluid absorption rate. Inhibition of peritoneal AGE accumulation prevented those functional and structural damages to the peritoneum.

Animals↗

Power generation from four skeletal muscle configurations. Design implications for a muscle powered cardiac assist device.

The development of long term cardiac assist devices is currently limited by the lack of an appropriate totally implantable power source. Transformed fatigue resistant skeletal muscle has been proposed as such a power source. The goal of this study was to determine the optimal latissimus dorsi muscle (LDM) configuration capable of obtaining maximum power output. Four separate in situ configurations were prepared: a latex compliance chamber placed between the LDM and chest wall (Sub-Dorsi), a chamber wrapped in a skeletal muscle ventricle (Circular), linear measurements from the thoracolumbar origin (Linear Origin), and linear measurements from the humeral insertion (Linear Insertion). A device was designed to measure the power output from each configuration in watts per kilogram of muscle. Eight LDMs were acutely studied at varying levels of pre-load. Performance characteristics were measured in each configuration. Peak power outputs were as follows: Sub-Dorsi: 8.3 +/- 1.6 W/kg at 50 cc or 11.6 N pre-load; Circular: 16.4 +/- 6.2 W/kg at 50 cc or 16.9 N; Linear Origin: 47.1 +/- 4.4 W/kg at 23.4 N; and Linear Insertion generated 59.9 +/- 12.1 W/kg at 26 N. Analysis of variance comparison revealed a significance of p < 0.0001. A linear oriented LDM is capable of generating maximal power output. Confirmation of these findings in transformed, conformed, fatigue resistant muscle will provide important performance information essential for the optimal design of implantable muscle powered ventricular assist systems.

Animals↗